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Current
Cardiology Reviews
ISSN: 1573-403X
Current Cardiology Reviews
Volume 4, Number 2, May 2008
Contents
Cellular Cardiomyoplasty and Cardiac Regeneration
Pp. 72-80
Lakshmana Pendyala, Traci Goodchild, Radhika
R. Gadesam, Jack Chen, Nicolas Chronos and
Dongming Hou
[Abstract]
Staged Starnes Operation Preserving Patent Ductus
Arteriosus for Neonates with Ebstein’s Anomaly and Pulmonary
Atresia Pp. 81-83
Yoichi Kawahira, Kyoichi Nishigaki, Hideto Ozawa and
Tsugutoshi Suzuki
[Abstract]
The Role of Glycoprotein IIb/IIIa Inhibitors-
A Promise Not Kept? Pp. 84-91
Edo Kaluski
[Abstract]
Chronic Heart Failure and Exercise Intolerance:
The Hemodynam0ic Paradox Pp. 92-100
Kent R. Nilsson Jr., Brian D. Duscha, Patrick M. Hranitzky
and William E. Kraus
[Abstract]
Critical Review of the Ankle Brachial Index
Pp. 101-106
Tahir H. Khan, Falahat A. Farooqui and
Khusrow Niazi
[Abstract]
The Involvement of Lysosomes in Myocardial Aging
and Disease Pp. 107-115
Alexei Terman, Tino Kurz, Bertil Gustafsson and
Ulf T. Brunk
[Abstract]
Cardiovascular Disease in Systemic Lupus Erythematosus:
The Role of Traditional and Lupus Related Risk Factors
Pp. 116-122
Carlos Borelli Zeller and Simone Appenzeller
[Abstract]
Neurocognitive Monitoring and Care During Pediatric
Cardiopulmonary Bypass—Current and Future Directions
Pp. 123-139
Jennifer K. Lee, R. Blaine Easley
and Kenneth M. Brady
[Abstract]
Peripheral Heart Blocks Associated with Myocardial
Infarcts: Clinical Diagnosis Based on Experimental Findings
Pp. 140-147
Gustavo A. Medrano, Alfredo de Micheli and Pedro
Iturralde
[Abstract]
Abstracts
[Back to top]
Cellular Cardiomyoplasty and Cardiac Regeneration
Lakshmana Pendyala, Traci Goodchild, Radhika
R. Gadesam, Jack Chen, Nicolas Chronos and
Dongming Hou
Despite of vast improvements in treatment, myocardial
infarction often leads to heart failure (HF) which remains
the leading cause of death in developed countries. Other than
heart transplantation, therapeutic options have a limited
role in improving out comes in patients with severe HF. It
is therefore no surprise that cardiac cell therapy has raised
many hopes as a novel therapeutic approach aimed at cardiac
myocyte replacement/regeneration termed “cellular cardiomyoplasty”.
However, the ideal source, cell type, critical cell number,
and mode of application for optimal therapeutic effect have
not been defined thus far. Recent observations of the beneficial
effect of cell transplantation in animal experiments have
generated tremendous excitement and stimulated clinical studies
suggesting that this approach is feasible, safe, and potentially
effective in humans. Cell-based myocardial regeneration is
currently being explored for a wide range of cardiac disease
states, including acute and chronic ischemic myocardial damage,
cardiomyopathy and as biological heart pacemakers. The main
purpose of this article is to review recent literature on
the use of various cells for the examination of their in
vitro cardiogenic potential and their in vivo
capacity to engraft and improve the functional properties
of the infarcted heart.
[Back to top]
Staged Starnes Operation Preserving Patent Ductus
Arteriosus for Neonates with Ebstein’s Anomaly and Pulmonary
Atresia
Yoichi Kawahira, Kyoichi Nishigaki, Hideto Ozawa
and Tsugutoshi Suzuki
We herein reported 2 successful neonates with Ebstein’s
anomaly and small pulmonary arteries undergoing Starnes operation
preserving the patent ductus arteriosus. Subsequent Blalock-Taussig
shunt was carried out 1 or 2 months after the first surgery.
One case had already undergone a successful Fontan operation,
and the other had a successful bidirectional Glenn shunt so
far. This staged Starnes strategy might be a safe and simple
choice for neonates with Ebstein’s anomaly and small
pulmonary arteries.
[Back to top]
The Role of Glycoprotein IIb/IIIa Inhibitors- A Promise
Not Kept?
Edo Kaluski
For over one decade Glycoproteins IIb/IIIa inhibitors
(GPI) have been administered to prevent coronary artery thrombosis.
Initially these agents were used for acute coronary syndromes
and subsequently as adjunctive pharmacotherapy for percutaneous
coronary interventions (PCIs).
Most benefit of GPI emerged from reduction of ischemic events:
mostly non-q-wave myocardial infarctions (NQWMIs) during PCI.
However, individual randomized clinical trials could not demonstrate
that any of these agents could significantly reduce mortality
in any clinical subset of patients. Studies of employing prolonged
oral GPI administration resulted in excessive death. The non-homogenous
statistically-significant reduction of ischemic endpoints
was accompanied by an excess of bleeding, vascular complications,
and thrombocytopenia. The clinical and ecomomic burden of
major bleeding and thrombocytopenia is substantial. The ACUITY
trial has initiate a new debate regarding the efficacy and
safety of GPI.
Selective “patient-tailored” use of GPI limited
to moderate-high risk PCI patients with low bleeding propensity
is suggested. Research of new algorithms emphasizing abbreviated
GPI administration, careful access site and bleeding surveillance,
in conjunction with lower doses of unfractionated heparin
or new and safer anti-thrombins may further enhance patient
safety.
[Back to top]
Chronic Heart Failure and Exercise Intolerance: The
Hemodynamic Paradox
Kent R. Nilsson Jr., Brian D. Duscha, Patrick M. Hranitzky
and William E. Kraus
Heart failure represents a major source of morbidity
and mortality in industrialized nations. As the leading hospital
discharge diagnosis in the United States in patients over
the age of 65, it is also associated with substantial economic
costs. While the acute symptoms of volume overload frequently
precipitate inpatient admission, it is the symptoms of chronic
heart failure, including fatigue, exercise intolerance and
exertional dyspnea, that impact quality of life. Over the
last two decades, research into the enzymatic, histologic
and neurohumoral alterations seen with heart failure have
revealed that hemodynamic derangements do not necessarily
correlate with symptoms. This “hemodynamic paradox”
is explained by alterations in the skeletal musculature that
occur in response to hemodynamic derangements. Importantly,
gender specific effects appear to modify both disease pathophysiology
and response to therapy. The following review will discuss
our current understanding of the systemic effects of heart
failure before examining how exercise training and cardiac
resynchronization therapy may impact disease course.
[Back to top]
Critical Review of the Ankle Brachial Index
Tahir H. Khan, Falahat A. Farooqui and
Khusrow Niazi
Ankle brachial index (ABI) has been utilized in the management
of peripheral arterial disease (PAD).ABI is a surrogate marker
of atherosclerosis and recent studies indicate its utility
as a predictor of future cardiovascular disease and all-cause
mortality. Even so, this critical test is underutilized. The
purpose of this review is to summarize available evidence
associated with ABI methodology variances, ABI usage in the
treatment of PAD, and ABI efficacy in predicting cardiovascular
disease. This review further evaluates how ABI is used in
the prognosis and follow-up of lower extremity arterial disease.We
reviewed the most current American College of Cardiology guidelines
for the management of PAD, the Trans Atlantic Intersociety
Consensus (TASC) working group recommendations, and searched
the Medline for the following words: ankle brachial index,
ABI sensitivity and specificity, and peripheral arterial disease.
The ABI is a simple, noninvasive clinical test that should
not only be applied to diagnose PAD, but also to provide important
prognostic information about future cardiovascular events.
Although the ABI has been employed in clinical practice for
some time, our review of various studies reveals a lack of
standardization regarding both the method of measuring ABI
and the cutoff point for abnormal ABI. It is extremely important
that we understand all aspects of this crucial test, as it
is now being recommended as part of a patient’s routine
health risk assessment.
[Back to top]
The Involvement of Lysosomes in Myocardial Aging and
Disease
Alexei Terman, Tino Kurz, Bertil Gustafsson and
Ulf T. Brunk
The myocardium is mainly composed of long-lived postmitotic
cells with, if there is any at all, a very low rate of replacement
through the division and differentiation of stem cells. As
a consequence, cardiac myocytes gradually undergo pronounced
age-related alterations which, furthermore, occur at a rate
that inversely correlates with the longevity of species. Basically,
these alterations represent the accumulation of structures
that have been damaged by oxidation and that are useless and
often harmful. These structures (so-called ‘waste’
materials), include defective mitochondria, aberrant cytosolic
proteins, often in aggregated form, and lipofuscin, which
is an intralysosomal undegradable polymeric substance. The
accumulation of ‘waste’ reflects the insufficient
capacity for autophagy of the lysosomal compartment, as well
as the less than perfect functioning of proteasomes, calpains
and other cellular digestive systems. Senescent mitochondria
are usually enlarged, show reduced potential over their inner
membrane, are deficient in ATP production, and often produce
increased amounts of reactive oxygen species. The turnover
of damaged cellular structures is hindered by an increased
lipofuscin loading of the lysosomal compartment. This particularly
restricts the autophagic turnover of enlarged, defective mitochondria,
by diverting the flow of lysosomal hydrolases from autophagic
vacuoles to lipofuscinloaded lysosomes where the enzymes are
lost, since lipofuscin is not degradable by lysosomal hydrolases.
As a consequence, aged lipofuscin-rich cardiac myocytes become
overloaded with damaged mitochondria, leading to increased
oxidative stress, apoptotic cell death, and the gradual development
of heart failure. Defective lysosomal function also underlies
myocardial degeneration in various lysosomal storage diseases,
while other forms of cardiomyopathies develop due to mitochondrial
DNA mutations, resulting in an accumulation of abnormal mitochondria
that are not properly eliminated by autophagy. The degradation
of iron-saturated ferritin in lysosomes mediates myocardial
injury in hemochromatosis, an acquired or hereditary disease
associated with iron overload. Lysosomes then become sensitized
to oxidative stress by the overload of low mass, redox-active
iron that accumulates when iron-saturated ferritin is degraded
following autophagy. Lysosomal destabilization is of importance
in the induction and/or execution of programmed cell death
(either classical apoptotic or autophagic), which is a common
manifestation of myocardial aging and a variety of cardiac
pathologies.
[Back to top]
Cardiovascular Disease in Systemic Lupus Erythematosus:
The Role of Traditional and Lupus Related Risk Factors
Carlos Borelli Zeller and Simone Appenzeller
Atherosclerosis is a chronic inflammatory disorder characterized
by immune cell activation, inflammation driven plaque formation
and subsequent destabilization. In other disorders of an inflammatory
nature, the chronic inflammatory state per se has been linked
to acceleration of the atherosclerotic process which is underlined
by an increased incidence of cardiovascular disease (CVD)
in disorders such as systemic lupus erythematosus (SLE), rheumatoid
arthritis (RA) and antiphopholipid (Hughes) syndrome (APS).
SLE is an autoimmune disease that may affect any organ. Premature
coronary heart disease has emerged as a major cause of morbidity
and mortality in SLE. In addition to mortality, cardiovascular
morbidity is also markedly increased in these patients, compared
with the general population. The increased cardiovascular
risk can be explained only partially by an increased prevalence
of classical risk factors for cardiovascular dis-ease; it
also appears to be related to inflammation. Inflammation is
increasingly being considered central to the pathogenesis
of atherosclerosis and an important risk factor for vascular
disease. Recent epidemiologic and pathogenesis studies have
suggested a great deal in common between the pathogenesis
of prototypic autoimmune disease such as SLE and that of atherosclerosis.
[Back to top]
Neurocognitive Monitoring and Care During Pediatric
Cardiopulmonary Bypass—Current and Future Directions
Jennifer K. Lee, R. Blaine Easley and Kenneth
M. Brady
Neurologic injury in patients with congenital heart disease
remains an important source of morbidity and mortality. Advances
in surgical repair and perioperative management have resulted
in longer life expectancies for these patients. Current practice
and research must focus on identifying treatable risk factors
for neurocognitive dysfunction, advancing methods for perioperative
neuromonitoring, and refining treatment and care of the congenital
heart patient with potential neurologic injury. Techniques
for neuromonitoring and future directions will be discussed.
[Back to top]
Peripheral Heart Blocks Associated with Myocardial
Infarcts: Clinical Diagnosis Based on Experimental Findings
Gustavo A. Medrano, Alfredo de Micheli and Pedro
Iturralde
Septal necrosis + peripheral left blocks. Because of
an extensive septal necrosis, the manifestation of the initial
ventricular activation forces decreases in the precordial
leads. With left bifascicular block (LASB + LPSB), the first
ventricular activation forces become more evident and the
electrical signs of septal necrosis can be concealed. In the
presence of a trifascicular block, manifestation of the first
ventricular electromotive forces diminishes again and the
electrical signs of septal necrosis
become evident once more. Small Q waves are present in leads
V1 to V4.
Extensive anterior necrosis + peripheral blocks. This necrosis
is manifested by QS complexes from V2
to V6. An associated left
bifascicular block reduces the electrical manifestation of
dead tissue: QS complexes persist only in V3
and V4. In turn, a
coexisting trifascicular block causes the presence of QS complexes
from V2 to V5.
Posteroinferior necrosis + peripheral blocks. Electromotive
forces of the ventricular activation shift upward, due to
a posteroinferior necrosis and QS or QR complexes are recorded
in leads aVF, II and III. An associated left bifascicular
block displaces the main electromotive forces downward, posteriorly
and to the left, due to a delay of the posteroinferior activation
fronts. The ventricular complexes become positive and wider
in all leads, reflecting the potential variations of the inferior
portions of the left ventricle: aVF, II, III, sometimes V5
and V6. Consequently, the
electrical signs of necrosis are reduced or abolished. Due
to a trifascicular block, wide and slurred QS complexes are
recorded in aVF, II, III and sometimes in V5
and V6.
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